EFFECTS OF DEVELOPMENTAL EXPOSURE TO INDOLE-3-CARBINOL OR 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN ON REPRODUCTIVE POTENTIAL OF MALE-RAT OFFSPRING

Citation
C. Wilker et al., EFFECTS OF DEVELOPMENTAL EXPOSURE TO INDOLE-3-CARBINOL OR 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN ON REPRODUCTIVE POTENTIAL OF MALE-RAT OFFSPRING, Toxicology and applied pharmacology, 141(1), 1996, pp. 68-75
Citations number
51
Categorie Soggetti
Pharmacology & Pharmacy",Toxicology
ISSN journal
0041008X
Volume
141
Issue
1
Year of publication
1996
Pages
68 - 75
Database
ISI
SICI code
0041-008X(1996)141:1<68:EODETI>2.0.ZU;2-C
Abstract
Treatment of pregnant female Sprague-Dawley rats on Gestational Day 15 with a single oral dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0.5, 1.0, or 2.0 mu g/kg) or indole-3-carbinol (I3C, 1.0 or 100 mg/k g), an aryl hydrocarbon (Ah) receptor agonist which is found in crucif erous vegetables, resulted in reproductive abnormalities in the male o ffspring (three to five litters in each treatment group). Anogenital d istance and crown to rump length were altered by both compounds; howev er, the timing of the effects (Day 1 or 5) was variable and the respon ses were not necessarily dose-dependent. In 62-day-old offspring, semi nal vesicle (24 to 26%), prostate (32 to 44%), testicular parenchymal (14%), and epididymal weight (19%) were decreased by one or more doses of TCDD. In contrast, I3C at one or more doses decreased daily sperm production/g testicular parenchyma (13 to 20%) and daily sperm product ion/testis (22%). Total number of sperm in the epididymis was signific antly decreased (30 to 33%) in rats perinatally exposed to TCDD and th is was due to a decreased (49 to 51%) number of sperm in the tail of t he epididymis. Perinatal exposure to I3C did not affect any of these p arameters. TCDD did not affect epididymal transit time of sperm throug h the complete epididymis at any of the doses (0.5 to 2.0 mu g/kg). Ho wever, at the two highest doses (1.0 and 2.0 mu g/kg), TCDD increased epididymal transit rate of sperm through the tail of the epididymis by 33 and 37%, respectively. In contrast, primarily due to decreased tra nsit rate (39%) of sperm through the head plus body of the epididymis, I3C (1 mg/kg) significantly increased total epididymal transit time b y 31%. In conclusion, perinatal exposure of pregnant rats to I3C, an A h receptor agonist similar to TCDD, causes reproductive abnormalities in male rat offspring; however, I3C and TCDD elicited both common and different responses. (C) 1996 Academic Press, Inc.